Dry Eye Disease (“DED”) is a condition that affects millions of people worldwide. The etiology of DED is becoming increasingly well understood. DED is progressive in nature, and results from the disruption of the natural tear film on the surface of the eye (e.g., the ocular surface). Such disruption may prevent healthy gas exchange and nutrient transport for the ocular surface, promote cellular desiccation, and/or may create a poor refractive surface for vision. The disruption of the natural tear film typically results from one or more of 1) insufficient aqueous tear production from the lacrimal glands (e.g., caused by secondary to post-menopausal hormonal deficiency, auto-immune disease, LASIK surgery, etc.), and/or 2) excessive evaporation of aqueous tears resulting from dysfunction of the meibomian glands. Low tear volume may cause a hyperosmolar environment that may induce an inflamed state of the ocular surface. This inflammatory response may induce apoptosis of ocular surface cells which in turn prevent proper distribution of the tear film on the ocular surface. Accordingly, any available tear volume delivered to the ocular surface may be rendered less effective. This may initiate a vicious cycle in which more inflammation can ensue, causing more ocular surface cell damage, etc. Additionally, the neural control loop, which controls reflex tear activation, may be disrupted because the sensory neurons in the ocular surface are damaged. As a result, fewer tears may be secreted and a second vicious cycle may develop that results in further progression of the disease (e.g., fewer tears may cause nerve cell loss, which may result in even fewer tears, etc.)
DED can result in ocular discomfort, visual disturbance, and/or a reduction in vision-related quality of life. Activities such as, e.g., driving, computer use, housework, and reading are often negatively impacted by DED. Subjects with severe cases of DED are at risk for serious ocular health deficiencies such as, e.g., corneal ulceration, and can experience a quality of life deficiency comparable to that of moderate to severe angina.
There is a wide spectrum of treatments for DED including: artificial tear substitutes, ointments, gels, warm compresses, environmental modification, topical cyclosporine, omega-3 fatty acid supplements, punctal plugs, moisture chamber goggles, punctal cautery, systemic cholinergic agonists, systemic anti-inflammatory agents, mucolytic agents, autologous serum tears, PROSE scleral contact lenses, and tarsorrhaphy. While current treatment options for DED are numerous, such treatment options have limited effectiveness and generally provide only mild symptom relief or improvement in ocular health over a short period of time.
The systems, devices, and methods of the current disclosure may rectify some of the deficiencies described above or address other aspects of the prior art.